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insulin secretion and action Flashcards

1
Q

what is the normal range for fasting glucose?

A

3.5-5.5mmol/L

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2
Q

what are the main roles of insulin?

A
  • High glucose levels -Removal of glucose from blood (transport)
  • Synthesis of glycogen and triglycerides (to store energy)
  • Inhibition of processes that release glucose/fatty acids
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3
Q

what happens in low glucose when insulin secretion is inhibited?

A
  • Low glucose levels –No glucose transport
  • Glycogen and triglycerides are not synthesised anymore
  • Processes that release glucose/fatty acids are not inhibited anymore
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4
Q

what is the main hormone controlling blood glucose levels during fasting?

A

glucagon

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5
Q

how many amino acids in a glucagon peptide?

A

29

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6
Q

describe how the synthesis of glucagon occurs

A

preproglucagon –> proglucagon –> pancreatic a-cells

or proglucagon can also undergo post-translational processes –> L-intestinal cells in the brain

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7
Q

what stimulates glucagon secretion?

A
  • Low blood glucose levels – normal fasting levels of glucose: 80-90mg/100ml
  • Increased blood amino acids – especially alanine and arginine
  • Exercise – in exhaustive exercise blood conc of glucagon increases 4.5 fold
  • Increase in intracellular calcium triggers an increase in glucagon
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8
Q

what inhibits glucagon secretion?

A

insulin

somatostatin

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9
Q

what type of receptor is the glucagon receptor?

A

GPCR - 7 transmembrane domains

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10
Q

explain how glucagon activates the receptor?

A
  • Dissociation of the trimer upon ligand binding to the receptor activates the signalling cascade - In the absence of glucose, trimer is assembled
  • When glucagon binds, a-subunit dissociates and can activate a cyclase - makes cAMP
  • cAMP triggers activation of the cascade
  • Activates PKA which activates phosphorylase
  • Only when the ligand binds, there’s production of cAMP
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11
Q

how can insulin regulate glucagon signalling?

A
  • Further regulation by insulin: insulin can switch glucagon-dependent signalling off
  • Insulin can break down cAMP to 5’ AMP by activating phosphodiesterase
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12
Q

describe metabolism during fasting?

A
  • Reduced glucose levels – no insulin secretion
  • Glycogenolysis isn’t inhibited
  • No glucose transport
  • Glycogen and triglycerides are not synthesised anymore
  • Processes that release glucose/fatty acids are NOT INHIBITED
  • Liver releases glucose into the bloodstream
  • Gluconeogenesis – synthesis of new glucose – is stimulated by glucagon in the liver
  • Lipolysis is not inhibited by insulin
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13
Q

how does glucagon increase gluconeogenesis and inhibit glycolysis in the liver?

A
  • Increases amino acid uptake by liver cells
  • Inhibition of PFK-1 (mediated by cAMP/PKA)
  • Inhibition of pyruvate kinase (mediated by cAMP/PKA)
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14
Q

what is lipolysis?

A

breaking down of triglycerides to FFAs and glycerol

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15
Q

what effect does HSL have on lipolysis?

A

increases lipolysis

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16
Q

what inhibits and activates HSL?

A

HSL inhibited by insulin and activated by glucagon/PKA

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17
Q

what effect does malonyl-CoA have on beta oxidation?

A

• Malonyl-CoA inhibits transport of FFAs into the mitochondria by CPT-1 therefore inhibiting B-oxidation

18
Q

what effect does glucagon have on CPT-1?

A

stimulates it

19
Q

how do ketone bodies form during fasting?

A

Accumulation of Acetyl-CoA that can’t enter TCA cycle is converted into KETONE BODIES

20
Q

when are catecholamines released?

A

Short term stress response - Released in response to stress and hypoglycaemia

21
Q

what are catecholamines?

A

Monoamines synthesised from phenylalanine and tyrosine

22
Q

what effect do catecholamines have?

A

• Increase HR and BP, causes liver to convert glycogen to glucose, dilation of bronchioles etc

23
Q

which cells secrete glucocorticoids and other steroids?

A

cortex cells

24
Q

how are cortex cells adapted for steroid hormone synthesis?

A

have many LDL receptors which enables cholesterol uptake

25
Q

what stimulates cortisol release?

A

secreted in response to adrenocorticotropic hormone (ACTH) from the pituitary - -ve feedback loop

26
Q

what effects do cortisol have on metabolism?

A
  • Enhances gluconeogenesis
  • Inhibits glucose uptake and utilisation
  • Stimulates muscle proteolysis
  • Stimulates adipose-tissue lipolysis  rapid mobilisation of amino acids and fatty acids from cellular stores
27
Q

what is the role of cortisol in stress and inflammation?

A
  • Cortisol is important in resisting stress and inflammation e.g. from trauma, infection, intense heat or cold, surgery or almost any debilitating disease
  • Helps maintain BP and it supresses inflammation
28
Q

what can happen if cortisol levels are elevated for a prolonged time?

A

can induce proteolysis and muscle wasting

29
Q

what are thyroxine (T4) and Triiodothyronine (T3) ?

A

iodinated thryonines

30
Q

what do T3 and T4 do?

A

• Activate nuclear receptors and transcription of large number of genes

31
Q

which is more potent? T3 or T4?

A

T3 is about 4 times more potent than T4

32
Q

which is present in smaller quantities - T3 or T4?

A

T3

33
Q

what are the metabolic actions of thyroid hormones?

A
  • increase in the number and activity of the mitochondria
  • stimulation of carbohydrate metabolism
  • stimulation of fat metabolism
  • leads to increased basal metabolic rate
34
Q

how do thyroid hormones stimulate carbohydrate metabolism?

A

o Rapid glucose uptake
o Enhanced glycolysis and gluconeogenesis
o Increased insulin secretion

35
Q

how is fat metabolism stimulated?

A

o Lipid mobilised rapidly from fat tissue

o Increased fatty acids concentration in the plasma

36
Q

what are incretins?

A

group of GI hormones

37
Q

what are the functions of GLP-1?

A

o Inhibits glucagon secretion and hepatic glucose production
o Augments glucose-induced insulin secretion
o Slows gastric e,ptying
o Promotes satiety
o Increases insulin biosynthesis
o Promotes B-cell differentiation

38
Q

what can cause hypoglycaemia?

A

o High insulin doses
o Alcohol excess – inhibits gluconeogenesis
o Insulinoma – tumour of pancreatic B cells
o Excessive exercise – leading to increased glucose utilisation
o Reactive hypoglycaemia – excessive insulin secretion in response to a high carbohydrate meal in pre-diabetic condition

39
Q

what are symptoms of hypoglycaemia?

A
  • Confusion, disorientation, convulsion, fitting, seizures, loss of consciousness, coma
  • Autonomic symptoms
  • Neuroglycopaenic symtpoms; difficulty concentrating, confusion, weakness, drowsiness, vision changes, difficulty speaking, dizziness, tiredness
  • Autonomic symptoms; Trembling, palpitation, sweating, anxiety, hunger, tingling
40
Q

what is secreted in prolonged hypoglycaemia?

A

• Growth hormone and cortisol are secreted – decrease rate of glucose utilisation

41
Q

what are the consequences of prolonged hypoglycaemia?

A

o Neuroglycopaenia – shortage of glucose for the brain
o Prolonged and repeated hypoglycaemia may produce permanent brain damage
o Loss of cognitive function, seizures and coma

42
Q

what can cause severe hypoglycaemia?

A

• Can occur in patients using blood glucose lowering medication or prandial glucose regulators as a result of;
o Missed or delayed meal
o Overdose medication
o Exercise (without adjustment in medication)
o Alcohol assumption

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